Dual effects of 8-Br-cAMP on differentiation and apoptosis of human esophageal cancer cell line Eca-109

Wang, Hongmei; Naigang, Zheng; Wu, Jiahui; Gong, Chang; Wang, Yiling

doi:10.3748/wjg.v11.i41.6538

Cited by 14 publications

(11 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Contributing mechanisms include G1 and G2/M cell cycle arrest (Ogawa, et al, 2002), mitochondrial depolarization, release of cytochrome c into the cytosol, and caspase-9 and -3 activation (Moon and Lerner, 2003). Elevation of cAMP concentration has also been shown to inhibit cell growth and induce apoptosis in other cancer cell lines such as retinoblastoma cells (Fassina, et al, 1997), papilloma cells (Marko, et al, 1998), glioma cells (Chen, et al, 2002), neuroblastoma cells (Kumar, et al, 2004), and esophageal cancer cells (Wang, et al, 2005). In cancer cell lines this effect of PDE-IV inhibition is an obvious area of interest since halting growth of these cells is a much-desired therapeutic goal.…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, in the treatment of bronchial asthma, PDE inhibition is thought to be an important mechanism of the anti-inflammatory actions of theophylline. Theophylline and rolipram have been shown to increase eosinophil intracellular cAMP concentrations and inhibit eosinophil survival (Momose, et al, 1998, Takeuchi, et al, 2002, Wang, et al, 2005). Recently it has been demonstrated that cAMP elevation resulted in significant inhibition of colony growth and induced apoptosis of progenitor cells in asthmatics, but not in normal subjects.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Glial restricted precursor cell transplant with cyclic adenosine monophosphate improved some autonomic functions but resulted in a reduced graft size after spinal cord contusion injury in rats

Nout

Culp²,

Schmidt

et al. 2011

Experimental Neurology

View full text Add to dashboard Cite

Transplantation of glial restricted precursor (GRP) cells has been shown to reduce glial scarring after spinal cord injury (SCI) and, in combination with neuronal restricted precursor (NRP) cells or enhanced expression of neurotrophins, to improve recovery of function after SCI. We hypothesized that combining GRP transplants with rolipram and cAMP would improve functional recovery, similar to that seen after combining Schwann cell transplants with increasing cAMP. A short term study, 1)uninjured control, 2)SCI+vehicle, and 3)SCI+cAMP, showed that spinal cord [cAMP] were increased 14 days after SCI. We used 51 male rats subjected to a thoracic SCI for a 12-week survival study: 1)SCI+vehicle, 2)SCI+GRP, 3)SCI+cAMP, 4)SCI+GRP+cAMP, and 5)uninjured endpoint age-matched control (AM). Rolipram was administered for 2 weeks after SCI. At 9 days after SCI, GRP transplantation and injection of dibutyryl-cAMP into the spinal cord were performed. GRP cells survived, differentiated, and formed extensive transplants that were well integrated with host tissue. Presence of GRP cells increased the amount of tissue in the © 2010 Elsevier Inc. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptExp Neurol. Author manuscript; available in PMC 2012 January 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript lesion; however, cAMP reduced the graft size. White matter sparing at the lesion epicenter was not affected. Serotonergic input to the lumbosacral spinal cord was not affected by treatment, but the amount of serotonin immediately caudal to the lesion was reduced in the cAMP groups. Using telemetric monitoring of corpus spongiosum penis pressure we show that the cAMP groups regained the same number of micturitions per 24 hrs when compared to the AM group, however, the frequency of peak pressures was increased in these groups compared to the AM group. In contrast, the GRP groups had similar frequency of peak pressures compared to baseline and the AM group. Animals that received GRP cells regained the same number of erectile events per 24 hrs compared to baseline and the AM group. Since cAMP reduced the GRP transplant graft, and some modest positive effects were seen that could be attributable to both GRP or cAMP, future research is required to determine how cAMP affects survival, proliferation, and / or function of progenitor cells and how this is related to function. cAMP may not always be a desirable addition to a progenitor cell transplantation strategy after SCI.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Glial restricted precursor cell transplant with cyclic adenosine monophosphate improved some autonomic functions but resulted in a reduced graft size after spinal cord contusion injury in rats

Nout

Culp²,

Schmidt

et al. 2011

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…It has been shown to inhibit proliferation, induce differentiation and apoptosis in a malignant glioma cell line (A-172) and an esophageal cancer cell line (Eca-109) [36,37]. Modulation of the cAMP/PKA pathway may thus represent a possible target site for treating malignant tumors and 8-Br-cAMP meets this criteria in a clinical setting.…”

Section: Discussionmentioning

confidence: 99%

A Cyclic AMP Analog, 8-Br-cAMP, Enhances the Induction of Pluripotency in Human Fibroblast Cells

Wang

Adjaye

2010

Stem Cell Rev and Rep

View full text Add to dashboard Cite

Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by ectopic expression of four transcription factors. However, the efficiency of human iPS cell generation is extremely low and therefore elucidating the mechanisms underlying cellular reprogramming is of prime importance. We demonstrate that 8-Bromoadenosine 3', 5'-cyclic monophosphate (8-Br-cAMP) improves the reprogramming efficiency of human neonatal foreskin fibroblast (HFF1) cells transduced with the four transcription factors by 2-fold. The combination of 8-Br-cAMP and VPA synergistically increases the efficiency to 6.5-fold. The effect of 8-Br-cAMP or VPA may in part be due to the up-regulation of cytokine-related and inflammatory pathways. Remarkably, the synergistic effect of 8-Br-cAMP and VPA on cellular reprogramming may be due to the transient decrease of p53 protein during the early stages of reprogramming. However, it could also be due to additional differentially regulated genes and pathways such as the up-regulation of cytokine-related, inflammatory pathways and self-renewal supporting gene, namely cyclin-encoding CCND2, and the associated genes CCNA1 and CCNE1. Conversely, we also see the down-regulation of the p53 (CCNB2, GTSE1, SERPINE1) and cell cycle (PLK1, CCNB2) pathways. Our data demonstrates that a cyclic AMP analog, 8-Br-cAMP, enhances the efficiency of cellular reprogramming. In addition, 8-Br-cAMP and VPA have a synergistic effect on cellular reprogramming, which may be in part due to the transient down-regulation of the p53 signaling pathway during the early stages of reprogramming.

show abstract

“…Among PGE2 receptors, PTGER2 has the most potential for elevating intracellular cAMP concentrations (Regan, 2003). Since elevated levels of cAMP are associated with decreased proliferation and increased differentiation or apoptosis in several types of cells including glioblastoma cells (Chen et al, 1998), esophageal squamous cell carcinomas (Wang et al, 2005b), and hippocampal cells (Takadera et al, 2004), we speculate that PTGER2-mediated production of intracellular cAMP may contribute to the growth-inhibitory effect of restored PTGER2 in NB cells lacking endogenous expression of the gene. In our experiments a PTGER2-specific agonist increased intracellular cAMP levels and exerted growth inhibitory effects, at least partly by inducing apoptosis, in stable PTGER2 transfectants established from the SJ-N-CG cell line, although G 0 -G 1 arrest but not apoptosis was predominantly observed in PTGER2 transfectants under low-serum condition without butaprost treatment.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic silencing of prostaglandin E receptor 2 (PTGER2) is associated with progression of neuroblastomas

et al. 2007

View full text Add to dashboard Cite

We previously identified a cluster of prostanoid receptor genes, prostaglandin D2 receptor (PTGDR) and prostaglandin E receptor 2 (PTGER2), as possible targets for DNA methylation in advanced types of neuroblastoma (NB) using bacterial artificial chromosome array-based methylated CpG island amplification method. Among them, in this study, we found that PTGER2 was frequently silenced in NB cell lines, especially in those with MYCN amplification, through epigenetic mechanisms. In NB cell lines, DNA methylation pattern within a part of CpG island was inversely correlated with PTGER2 expression, and histone H3 and H4 deacetylation and histone H3 lysine 9 methylation within the putative promoter region were more directly correlated with silencing of this gene. Methylation of PTGER2 was observed more frequently in advancedtype of primary NBs compared with early-stage tumors. Growth of NB cells lacking endogenous PTGER2 expression was inhibited by restoration of the gene product by transient and stable transfection. A PTGER2-selective agonist, butaprost, increased intracellular cyclic adenosine monophosphate (cAMP) level, inhibited cell growth and induced apoptosis of NB cells stably expressing exogenous PTGER2. 8-Bromo-cAMP also inhibited growth of NB cells lacking PTGER2 expression, but not cells expressing this gene. Taken together, it is suggested that NB cells may lose responsiveness to PTGER2-mediated growth inhibition/ apoptosis through epigenetic silencing of PTGER2 and/ or disruption of downstream cAMP-dependent pathway during the neuroblastomagenesis.

show abstract

Dual effects of 8-Br-cAMP on differentiation and apoptosis of human esophageal cancer cell line Eca-109

Cited by 14 publications

References 15 publications

Glial restricted precursor cell transplant with cyclic adenosine monophosphate improved some autonomic functions but resulted in a reduced graft size after spinal cord contusion injury in rats

Glial restricted precursor cell transplant with cyclic adenosine monophosphate improved some autonomic functions but resulted in a reduced graft size after spinal cord contusion injury in rats

A Cyclic AMP Analog, 8-Br-cAMP, Enhances the Induction of Pluripotency in Human Fibroblast Cells

Epigenetic silencing of prostaglandin E receptor 2 (PTGER2) is associated with progression of neuroblastomas

Contact Info

Product

Resources

About